Anti-Oligodendrocyte Marker O4 Antibody, Clone 81

Mouse monoclonal IgM antibody against human, mouse, rat oligodendrocyte marker O4

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Anti-Oligodendrocyte Marker O4 Antibody, Clone 81

Mouse monoclonal IgM antibody against human, mouse, rat oligodendrocyte marker O4, unconjugated

50 µg
Catalog #60053
611 USD

Overview

O-Antigens are expressed on oligodendrocytes during differentiation and on mature oligodendrocytes in the central nervous system. O4 is formed during postnatal development and is a marker for cell bodies and processes of oligodendrocytes types I and II. O4 is expressed in pro-oligodendrocytes, however, it is not found on O-2A-progenitor cells.
Subtype:
Primary Antibodies
Target Antigen:
Oligodendrocyte Marker O4
Alternative Names:
CLDN11, Claudin-11, Oligodendrocyte transmembrane protein
Reactive Species:
Human; Mouse; Rat; Pig
Conjugation:
Unconjugated
Host Species:
Mouse
Cell Type:
Neural Stem and Progenitor Cells; Neural Cells, PSC-Derived
Application:
Flow Cytometry; Immunocytochemistry; Immunohistochemistry; Immunofluorescence
Area of Interest:
Neuroscience
Clone:
81
Gene ID:
5010
Isotype:
IgM

Scientific Resources

Educational Materials

(4)

Product Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Data and Publications

Publications

(1)
Human Molecular Genetics 2011 SEP

Modeling neuronal defects associated with a lysosomal disorder using patient-derived induced pluripotent stem cells.

Lemonnier T et al.

Abstract

By providing access to affected neurons, human induced pluripotent stem cells (iPSc) offer a unique opportunity to model human neurodegenerative diseases. We generated human iPSc from the skin fibroblasts of children with mucopolysaccharidosis type IIIB. In this fatal lysosomal storage disease, defective α-N-acetylglucosaminidase interrupts the degradation of heparan sulfate (HS) proteoglycans and induces cell disorders predominating in the central nervous system, causing relentless progression toward severe mental retardation. Partially digested proteoglycans, which affect fibroblast growth factor signaling, accumulated in patient cells. They impaired isolation of emerging iPSc unless exogenous supply of the missing enzyme cleared storage and restored cell proliferation. After several passages, patient iPSc starved of an exogenous enzyme continued to proliferate in the presence of fibroblast growth factor despite HS accumulation. Survival and neural differentiation of patient iPSc were comparable with unaffected controls. Whereas cell pathology was modest in floating neurosphere cultures, undifferentiated patient iPSc and their neuronal progeny expressed cell disorders consisting of storage vesicles and severe disorganization of Golgi ribbons associated with modified expression of the Golgi matrix protein GM130. Gene expression profiling in neural stem cells pointed to alterations of extracellular matrix constituents and cell-matrix interactions, whereas genes associated with lysosome or Golgi apparatus functions were downregulated. Taken together, these results suggest defective responses of patient undifferentiated stem cells and neurons to environmental cues, which possibly affect Golgi organization, cell migration and neuritogenesis. This could have potential consequences on post-natal neurological development, once HS proteoglycan accumulation becomes prominent in the affected child brain.
STEMCELL TECHNOLOGIES INC.’S QUALITY MANAGEMENT SYSTEM IS CERTIFIED TO ISO 13485. PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED.